Fungal microbiota dysbiosis in IBD

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Abstract

Objective

The bacterial intestinal microbiota plays major roles in human physiology and IBDs. Although some data suggest a role of the fungal microbiota in IBD pathogenesis, the available data are scarce. The aim of our study was to characterise the faecal fungal microbiota in patients with IBD.

Design

Bacterial and fungal composition of the faecal microbiota of 235 patients with IBD and 38 healthy subjects (HS) was determined using 16S and ITS2 sequencing, respectively. The obtained sequences were analysed using the Qiime pipeline to assess composition and diversity. Bacterial and fungal taxa associated with clinical parameters were identified using multivariate association with linear models. Correlation between bacterial and fungal microbiota was investigated using Spearman's test and distance correlation.

Results

We observed that fungal microbiota is skewed in IBD, with an increased Basidiomycota/Ascomycota ratio, a decreased proportion of Saccharomyces cerevisiae and an increased proportion of Candida albicans compared with HS. We also identified disease-specific alterations in diversity, indicating that a Crohn's disease-specific gut environment may favour fungi at the expense of bacteria. The concomitant analysis of bacterial and fungal microbiota showed a dense and homogenous correlation network in HS but a dramatically unbalanced network in IBD, suggesting the existence of disease-specific inter-kingdom alterations.

Conclusions

Besides bacterial dysbiosis, our study identifies a distinct fungal microbiota dysbiosis in IBD characterised by alterations in biodiversity and composition. Moreover, we unravel here disease-specific inter-kingdom network alterations in IBD, suggesting that, beyond bacteria, fungi might also play a role in IBD pathogenesis.

Related collections

Most cited references 30

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Interactions between commensal fungi and the C-type lectin receptor Dectin-1 influence colitis.

Iliyan Iliev, Vincent Funari, Kent D. Taylor … (2012)

The intestinal microflora, typically equated with bacteria, influences diseases such as obesity and inflammatory bowel disease. Here, we show that the mammalian gut contains a rich fungal community that interacts with the immune system through the innate immune receptor Dectin-1. Mice lacking Dectin-1 exhibited increased susceptibility to chemically induced colitis, which was the result of altered responses to indigenous fungi. In humans, we identified a polymorphism in the gene for Dectin-1 (CLEC7A) that is strongly linked to a severe form of ulcerative colitis. Together, our findings reveal a eukaryotic fungal community in the gut (the "mycobiome") that coexists with bacteria and substantially expands the repertoire of organisms interacting with the intestinal immune system to influence health and disease.

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Archaea and Fungi of the Human Gut Microbiome: Correlations with Diet and Bacterial Residents

Christian Hoffmann, Serena Dollive, Stephanie Grunberg … (2013)

Diet influences health as a source of nutrients and toxins, and by shaping the composition of resident microbial populations. Previous studies have begun to map out associations between diet and the bacteria and viruses of the human gut microbiome. Here we investigate associations of diet with fungal and archaeal populations, taking advantage of samples from 98 well-characterized individuals. Diet was quantified using inventories scoring both long-term and recent diet, and archaea and fungi were characterized by deep sequencing of marker genes in DNA purified from stool. For fungi, we found 66 genera, with generally mutually exclusive presence of either the phyla Ascomycota or Basiodiomycota. For archaea, Methanobrevibacter was the most prevalent genus, present in 30% of samples. Several other archaeal genera were detected in lower abundance and frequency. Myriad associations were detected for fungi and archaea with diet, with each other, and with bacterial lineages. Methanobrevibacter and Candida were positively associated with diets high in carbohydrates, but negatively with diets high in amino acids, protein, and fatty acids. A previous study emphasized that bacterial population structure was associated primarily with long-term diet, but high Candida abundance was most strongly associated with the recent consumption of carbohydrates. Methobrevibacter abundance was associated with both long term and recent consumption of carbohydrates. These results confirm earlier targeted studies and provide a host of new associations to consider in modeling the effects of diet on the gut microbiome and human health.

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Connecting dysbiosis, bile-acid dysmetabolism and gut inflammation in inflammatory bowel diseases.

Henri Duboc, Sylvie Rajca, Dominique Rainteau … (2013)

Gut microbiota metabolises bile acids (BA). As dysbiosis has been reported in inflammatory bowel diseases (IBD), we aim to investigate the impact of IBD-associated dysbiosis on BA metabolism and its influence on the epithelial cell inflammation response. Faecal and serum BA rates, expressed as a proportion of total BA, were assessed by high-performance liquid chromatography tandem mass spectrometry in colonic IBD patients (42) and healthy subjects (29). The faecal microbiota composition was assessed by quantitative real-time PCR. Using BA profiles and microbiota composition, cluster formation between groups was generated by ranking models. The faecal BA profiles in germ-free and conventional mice were compared. Direct enzymatic activities of BA biotransformation were measured in faeces. The impact of BA on the inflammatory response was investigated in vitro using Caco-2 cells stimulated by IL-1β. IBD-associated dysbiosis was characterised by a decrease in the ratio between Faecalibacterium prausntizii and Escherichia coli. Faecal-conjugated BA rates were significantly higher in active IBD, whereas, secondary BA rates were significantly lower. Interestingly, active IBD patients exhibited higher levels of faecal 3-OH-sulphated BA. The deconjugation, transformation and desulphation activities of the microbiota were impaired in IBD patients. In vitro, secondary BA exerted anti-inflammatory effects, but sulphation of secondary BAs abolished their anti-inflammatory properties. Impaired microbiota enzymatic activity observed in IBD-associated dysbiosis leads to modifications in the luminal BA pool composition. Altered BA transformation in the gut lumen can erase the anti-inflammatory effects of some BA species on gut epithelial cells and could participate in the chronic inflammation loop of IBD.

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Author and article information

Journal

Journal ID (nlm-ta): Gut

Journal ID (iso-abbrev): Gut

Journal ID (hwp): gutjnl

Journal ID (publisher-id): gut

Title: Gut

Publisher: BMJ Publishing Group (BMA House, Tavistock Square, London, WC1H 9JR )

ISSN (Print): 0017-5749

ISSN (Electronic): 1468-3288

Publication date (Print): June 2017

Publication date (Electronic): 3 February 2016

Volume: 66

Issue: 6

Pages: 1039-1048

Affiliations

[1 ]Sorbonne University—UPMC Univ Paris 06, INSERM ERL 1157, Avenir Team Gut Microbiota and Immunity, UMR 7203, Saint-Antoine Hospital , AP-HP, UPMC Univ Paris 06, Paris, France

[2 ]Micalis Institute, INRA, AgroParisTech, Université Paris-Saclay , Jouy-en-Josas, France

[3 ]Department of Gastroenterology, Saint Antoine Hospital , Paris, France

[4 ]Inflammation-Immunopathology-Biotherapy Department (DHU i2B), Paris, France

[5 ]Department of Epidemiology, Harvard School of Public Health , Boston, Massachusetts, USA

[6 ]ILTOO Pharma, iPEPS ICM, Hôpital Pitié Salpêtrière , Paris, France

[7 ]Department of Medical and Surgical Sciences, University of Bologna , Bologna, Italy

[8 ]Division of Infectious Diseases, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School , Boston, Massachusetts, USA

[9 ]Massachusetts Technology and Analytics , Brookline, Massachusetts, USA

Author notes

[Correspondence to ] Dr Harry Sokol, Service de Gastroentérologie et Nutrition, Hôpital Saint-Antoine, 184 rue du faubourg St Antoine, Paris 75571, cedex 12, France; harry.sokol@ 123456aphp.fr

Article

Publisher ID: gutjnl-2015-310746

DOI: 10.1136/gutjnl-2015-310746

PMC ID: 5532459

PubMed ID: 26843508

SO-VID: 08f81c31-0ece-425f-a598-323de55a1483

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License:

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